Hintergrund

The human complement system is, as part of the innate immune system, responsible for the defence against invading pathogens . Complement activation is tightly regulated, leading to the generation of a series of complement split products (such as C4d) from inactive precursor molecules that ultimately Iead to the destruction of invading pathogens and their clearance from the body. Split product C4d itself has been orphan Iigand wit h no known attributed function per se. However, in some studies it was associated with the autoimmune syndrome systemic Iupus erythematosus , and presence of C4d in renal allografts is an established marker of antibody-media ted graft rejection.

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Lösung

Complement split product C4d was found to be capable of triggering an anti­ inflammatory response or down-regulate a pro-inflammatory response, respectively , in an in vitro model of an inflammatory disease.C4d decreases production of the pro-inflammatory factors TNF-a and IL-6. Moreover, C4d inhibits the activation of dendritic cells (DC), key effector cells in the pathogenesis of inflammatory diseases . ln autoimmune diseases, such as psoriasis and rheumatoid arthritis , the activation Ievei and the number of DC were observed to be increased.